Eating the plate instead of the food
October 8, 2012 9:25 AM   Subscribe

With the possible exception of the Nobel awards, physicists seem to get all the press these days, whether they're doing quantum level work at the LHC, or cosmology via the latest satellite data. Biologists, not so much. It's too bad, because Richard Lenski is running one of the great evolutionary experiments of our time, and it's producing interesting results.

Lenski and his team have raised 55,000 generations of E. coli, the equivalent in human terms, of over a million years of evolution. These bacteria normally feed on glucose, a sugar, which is stabilized in solution by sodium citrate, not a chemical that E. coli can typically metabolize. In Lenski's lab, however, one strain has evolved to eat the citrate, not the glucose. Because Lenski deep-freezes samples every 500 generations. They were able to track the mutations that led to this change. One of my favorite science journalists, Carl Zimmer, has been following this work for over a decade with reports like the one above.

Lenski, who was awarded a MacArthur grant in 1996, combines ecology and genetics to create experiments that illustrate the role of population dynamics in evolution, and his research supports the "punctuated equilibrium" model suggested by Steven J Gould and Niles Eldridge. In addition to lab work showing evolution occurring "in the flesh", Lenski has also published work using computer simulations that advance understanding of evolutionary mechanisms.
posted by CheeseDigestsAll (34 comments total) 68 users marked this as a favorite

 
Previously
posted by Blasdelb at 9:30 AM on October 8, 2012 [1 favorite]


Lenski is the poor man who actually engaged Andrew Schlafly in an email dialog where Schlafly thought he could trap Lenski with a request for the "raw data". Either Lenski would refuse to turn over the data, which was publicly funded, thus proving the liberal conspiracy to enslave us all with "science", or he would turn it over and they'd get a chance to prove that natural selection hadn't really occurred. Lenski actually provides a good model for scientists dealing with people like Schlafly: Initially polite and helpful, but quickly calling bullshit on the attempted ambush.
posted by fatbird at 9:44 AM on October 8, 2012 [17 favorites]


That Lenski-Schlafly exchange was good for a few laughs, but I worry that it didn't change any minds.
posted by sneebler at 9:52 AM on October 8, 2012


As someone who works in a lab that does a lot of evolutionary biology work (albeit in a rather different vein) I've been exposed to some of Lenski's research and it's really fascinating stuff. He has a couple of papers which explore the idea that not only is mutation a primary driver of evolution, but that mutation rates themselves are targets of selection such that a population of organisms might evolve to have higher or lower mutation rates depending on environmental factors. Heady stuff. His poor students though, inoculating cell culture after cell culture, ad infinitum. It's tedious but very valuable and fruitful work.
posted by Scientist at 9:55 AM on October 8, 2012 [1 favorite]


In case it helps someone to hear a lay personish audio summary of his work,here it is.

I've read about his work before in antibiotic resistance (PDF) and found it fascinating.
posted by Wolfster at 9:56 AM on October 8, 2012


I should say that his work also speaks to the value of the kind of long-term, longitudinal studies that are so hard to get funded these days. Lenski can get grants to keep doing what he does because at this point he has a sterling track record of producing great research, but it's not an easy thing to get support for a career that involves doggedly pursuing the same set of questions in the same way for decades on end and which only starts yielding really interesting data around Year Ten.
posted by Scientist at 9:58 AM on October 8, 2012 [1 favorite]


That Lenski-Schlafly exchange was good for a few laughs, but I worry that it didn't change any minds.

Well, it cost Mr. Schlafly a few otherwise intelligent and qualified followers of Conservapedia. Between banning dissenters and wilful refusal to consider contrary opinions, he actually lost a significant (for Conservapedia) number of editors. He actually had microbiologists arguing with him, and drove them away.
posted by fatbird at 9:59 AM on October 8, 2012 [3 favorites]


Dr. Lenski, I have no idea what half of your words mean, but I'd like to subscribe to your newsletter just the same.
posted by Blue_Villain at 10:06 AM on October 8, 2012 [3 favorites]


Cases of evolution observed within a single human lifetime can be the final straw for some die-hard creationists.

I was talking to a highly conservative friend recently, and somehow evolution came up. To my surprise, she endorsed a version of the "microevolution not macroevolution" position. I brought up the Italian Wall Lizards of Pod Mrčaru. The story: in 1971 ten lizards were introduced to an island off the coast of Croatia by a group of scientists, but observations were interrupted by war. When scientists returned in 2008 to study the population, they discovered that the lizards were no longer insectivores, having switched to a largely vegetarian diet (plants going from 4-7% of their diet to 34-61%). They'd evolved cecal valves, segmenting their digestive tracts to give them fermentation chambers.

"Well, they're still lizards. It's not like they turned into cows."
"But that's exactly what happened!"
Stunned silence, wheels turning. Flawless victory.

It's a case so simple and straightforward that it burns away the usual ways of deflecting evidence and leaves only two options: acceptance and willfully plugging one's ears. Some people will pick option two, but that takes a certain amount of effort to sustain. On some level, they now know.
posted by justsomebodythatyouusedtoknow at 10:15 AM on October 8, 2012 [25 favorites]


Some people will pick option two, but that takes a certain amount of effort to sustain. On some level, they now know.

They now know that they hate you.
posted by benzenedream at 10:39 AM on October 8, 2012


I wonder how many bacteria they save from each of the every-500 generation samples. Are those a precious resource? I know you can grow more of them, but when you do, you're winding the generation clock forward -- you're not just making more of what was in that interesting vial.

Do grad students have to submit a research proposal: "I want to test X using 1µl of generation 12345." And they only get a sample of that generation if X is interesting enough to warrant using up whatever is left?
posted by spacewrench at 10:42 AM on October 8, 2012


If you grow more of a frozen generation, you're only advancing a generation or two up the line when the next frozen sample is +500.

This is awesome research.
posted by localroger at 10:47 AM on October 8, 2012


The Carl Zimmer article is particularly fascinating. Basically, he breaks it down to say that a happenstance mutation caused these bacteria to evolve to digest Citrate in oxygen, which is very rare. But, they only were able to effectively utilize and refine that ability because of previous happenstance mutations.

I think that evolution is not widely accepted partially because it is impossible to comprehend six billion years. Lab experiments like this show how such mutations and adaptations can happen on a simple, reproducible genome. Scale that up, and, to me at least, it makes sense that life as we know it is created from bacterial soup.

But it's a heck of a leap of faith to go from bacterial evolution to the development of multicellular species, so, I can understand why six billion years is hard to conceptualize. (Talk of six thousand years of Earth is where I get cranky and stop listening.)
posted by Turkey Glue at 10:49 AM on October 8, 2012 [2 favorites]


Yes, Zimmer's a treasure. Perhaps that should have been the FP link, but I wanted to give an overview of the experiment first. He also points out in that article, that a similar evolutionary mechanism turned a snake's pancreatic enzymes into venom.
posted by CheeseDigestsAll at 11:35 AM on October 8, 2012


So long as this thread is sticking around I think its pretty cool that metafilter is paying attention to Microbial Evolution again. Its a really cool, amazingly promising and oddly neglected field where evolutionary biologists tend to not understand microbiology well enough to do anything meaningful with it and microbiologists seem to mostly only play with it as an afterthought - but there is still so much amazing and fascinating work being done with it. Rich Lenski's long term experiment is amazingly awesome, but only seems to be getting the attention it has gotten because it sticks a very sharp stick in the eye of creationists, which hey no complaints or anything but not really what metafilter needs. Here is a pretty paired down collection of Blasdelb's favorite papers in microbial evolution, with the free access ones marked with *** so as not to tease you, each of which is very much on par with Lenski's work in terms of wow factor and amazingness. They have also been selected to present different aspects of the field, and while some knowledgable observers might claim a phage bias, I think that is totally defensible. As always if you would like copies of those papers that are not publicly available - for the purpose of this academic discussion that we are having - feel free to memail me with an email address I can send PDFs you want to.
Fitness of RNA virus decreased by Muller's ratchet. Nature. 348(6300):454-5.
Why sex exists remains an unsolved problem in biology. If mutations are on the average deleterious, a high mutation rate can account for the evolution of sex. One form of this mutational hypothesis is Muller's ratchet. If the mutation rate is high, mutation-free individuals become rare and they can be lost by genetic drift in small populations. In asexual populations, as Muller noted, the loss is irreversible and the load of deleterious mutations increases in a ratchet-like manner with the successive loss of the least-mutated individuals. Sex can be advantageous because it increases the fitness of sexual populations by re-creating mutation-free individuals from mutated individuals and stops (or slows) Muller's ratchet. Although Muller's ratchet is an appealing hypothesis, it has been investigated and documented experimentally in only one group of organisms--ciliated protozoa. I initiated a study to examine the role of Muller's ratchet on the evolution of sex in RNA viruses and report here a significant decrease in fitness due to Muller's ratchet in 20 lineages of the RNA bacteriophage phi 6. These results show that deleterious mutations are generated at a sufficiently high rate to advance Muller's ratchet in an RNA virus and that beneficial, backward and compensatory mutations cannot stop the ratchet in the observed range of fitness decrease.

***Mitigating Mutational Meltdown in Mammalian Mitochondria PLoS Biol 6(2): e35.
Mitochondria are remarkable microorganisms. About two billion years ago, their distant free-living ancestors hooked up with a truly foreign lineage of archaebacteria and started a genomic merger that led to the most successful coevolved mutualism on the planet: the eukaryotic cell. Along the way, evolving mitochondria lost a lot of genomic baggage, entrusted their emerging hosts with their own replication, sorted out genomic conflicts by following maternal inheritance, and have mostly abstained from sex and recombination. What mitochondria did retain was a subset of genes that encode critical components of the electron transport chain and ATP synthesis enzymes that carry out oxidative phosphorylation. Because mitochondria house the biochemical machinery that requires us to breathe oxygen, it was first assumed that mitochondrial genes would show very slow rates of molecular evolution. So it was big news almost 30 years ago when mitochondrial DNA (mtDNA) evolution was observed to be quite rapid [1]. How could the genes for a highly conserved and critical function sustain the consequences of high mutation pressure and permit rapid rates of nucleotide substitution between species? Without the benefits of recombination, where offspring can carry fewer mutations than either parent, mutations should accumulate in mitochondrial genomes through the random loss of less-mutated genomes, a process referred to as Muller's ratchet [2,3]. How have mitochondria avoided a mutational meltdown, or at least significant declines in fitness?

Adaptive radiation in a heterogeneous environment Nature 394, 69-72.
Successive adaptive radiations have played a pivotal role in the evolution of biological diversity. The effects of adaptive radiation are often seen but the underlying causes are difficult to disentangle and remain unclear. Here we examine directly therole of ecological opportunity and competition in driving genetic diversification. We use the common aerobic bacterium Pseudomonas fluorescens, which evolves rapidly under novel environmental conditions to generate a large repertoire of mutants. When provided with ecological opportunity (afforded by spatial structure), identical populations diversify morphologically, but when ecological opportunity is restricted there is no such divergence. In spatially structured environments, the evolution of variant morphs follows a predictable sequence and we show that competition among the newly evolved niche-specialists maintains this variation. These results demonstrate that the elementary processes of mutation and selection alone are suifficient to promote rapid proliferation of new designs and support the theory that trade-offs in competitive ability drive adaptive radiation.

Plasmids Spread Very Fast in Heterogeneous Bacterial Communities Genetics. 2002 Dec;162(4):1525-32.
Conjugative plasmids can mediate gene transfer between bacterial taxa in diverse environments. The ability to donate the F-type conjugative plasmid R1 greatly varies among enteric bacteria due to the interaction of the system that represses sex-pili formations (products of finOP) of plasmids already harbored by a bacterial strain with those of the R1 plasmid. The presence of efficient donors in heterogeneous bacterial populations can accelerate plasmid transfer and can spread by several orders of magnitude. Such donors allow millions of other bacteria to acquire the plasmid in a matter of days whereas, in the absence of such strains, plasmid dissemination would take years. This "amplification effect" could have an impact on the evolution of bacterial pathogens that exist in heterogeneous bacterial communities because conjugative plasmids can carry virulence or antibiotic-resistance genes.

Massive Horizontal Gene Transfer in Bdelloid Rotifers Science
Horizontal gene transfer in metazoans has been documented in only a few species and is usually associated with endosymbiosis or parasitism. By contrast, in bdelloid rotifers we found many genes that appear to have originated in bacteria, fungi, and plants, concentrated in telomeric regions along with diverse mobile genetic elements. Bdelloid proximal gene-rich regions, however, appeared to lack foreign genes, thereby resembling those of model metazoan organisms. Some of the foreign genes were defective, whereas others were intact and transcribed; some of the latter contained functional spliceosomal introns. One such gene, apparently of bacterial origin, was overexpressed in Escherichia coli and yielded an active enzyme. The capture and functional assimilation of exogenous genes may represent an important force in bdelloid evolution.

Sex increases the efficacy of natural selection in experimental yeast populations Nature
Why sex evolved and persists is a problem for evolutionary biology, because sex disrupts favourable gene combinations and requires an expenditure of time and energy1. Further, in organisms with unequal-sized gametes, the female transmits her genes at only half the rate of an asexual equivalent (the twofold cost of sex)2. Many modern theories that provide an explanation for the advantage of sex incorporate an idea originally proposed by Weismann more than 100 years ago: sex allows natural selection to proceed more effectively because it increases genetic variation3, 4, 5. Here we test this hypothesis, which still lacks robust empirical support, with the use of experiments on yeast populations. Capitalizing on recent advances in the molecular biology of recombination in yeast, we produced by genetic manipulation strains that differed only in their capacity for sexual reproduction. We show that, as predicted by the theory, sex increases the rate of adaptation to a new harsh environment but has no measurable effect on fitness in a new benign environment where there is little selection.

***Giant Marseillevirus highlights the role of amoebae as a melting pot in emergence of chimeric microorganisms PNAS
Giant viruses such as Mimivirus isolated from amoeba found in aquatic habitats show biological sophistication comparable to that of simple cellular life forms and seem to evolve by similar mechanisms, including extensive gene duplication and horizontal gene transfer (HGT), possibly in part through a viral parasite, the virophage. We report here the isolation of “Marseille” virus, a previously uncharacterized giant virus of amoeba. The virions of Marseillevirus encompass a 368-kb genome, a minimum of 49 proteins, and some messenger RNAs. Phylogenetic analysis of core genes indicates that Marseillevirus is the prototype of a family of nucleocytoplasmic large DNA viruses (NCLDV) of eukaryotes. The genome repertoire of the virus is composed of typical NCLDV core genes and genes apparently obtained from eukaryotic hosts and their parasites or symbionts, both bacterial and viral. We propose that amoebae are “melting pots” of microbial evolution where diverse forms emerge, including giant viruses with complex gene repertoires of various origins.

***High frequency of hotspot mutations in core genes of Escherichia coli due to short-term positive selection PNAS
Core genes comprising the ubiquitous backbone of bacterial genomes are not subject to frequent horizontal transfer and generally are not thought to contribute to the adaptive evolution of bacterial pathogens. We determined, however, that at least one-third and possibly more than one-half of the core genes in Escherichia coli genomes are targeted by repeated replacement substitutions in the same amino acid positions—hotspot mutations. Occurrence of hotspot mutations is driven by positive selection, as their rate is significantly higher than expected by random chance alone, and neither intragenic recombination nor increased mutability can explain the observed patterns. Also, commensal E. coli strains have a significantly lower frequency of mutated genes and mutations per genome than pathogenic strains. E. coli strains causing extra-intestinal infections accumulate hotspot mutations at the highest rate, whereas the highest total number of mutated genes has been found among Shigella isolates, suggesting the pathoadaptive nature of such mutations. The vast majority of hotspot mutations are of recent evolutionary origin, implying short-term positive selection, where adaptive mutations emerge repeatedly but are not sustained in natural circulation for long. Such pattern of dynamics is consistent with source-sink model of virulence evolution.

***Ancient, recurrent phage attacks and recombination shaped dynamic sequence-variable mosaics at the root of phytoplasma genome evolution PNAS
Mobile genetic elements have impacted biological evolution across all studied organisms, but evidence for a role in evolutionary emergence of an entire phylogenetic clade has not been forthcoming. We suggest that mobile element predation played a formative role in emergence of the phytoplasma clade. Phytoplasmas are cell wall-less bacteria that cause numerous diseases in plants. Phylogenetic analyses indicate that these transkingdom parasites descended from Gram-positive walled bacteria, but events giving rise to the first phytoplasma have remained unknown. Previously we discovered a unique feature of phytoplasmal genome architecture, genes clustered in sequence-variable mosaics (SVMs), and suggested that such structures formed through recurrent, targeted attacks by mobile elements. In the present study, we discovered that cryptic prophage remnants, originating from phages in the order Caudovirales, formed SVMs and comprised exceptionally large percentages of the chromosomes of ‘Candidatus Phytoplasma asteris’-related strains OYM and AYWB, occupying nearly all major nonsyntenic sections, and accounting for most of the size difference between the two genomes. The clustered phage remnants formed genomic islands exhibiting distinct DNA physical signatures, such as dinucleotide relative abundance and codon position GC values. Phytoplasma strain-specific genes identified as phage morons were located in hypervariable regions within individual SVMs, indicating that prophage remnants played important roles in generating phytoplasma genetic diversity. Because no SVM-like structures could be identified in genomes of ancestral relatives including Acholeplasma spp., we hypothesize that ancient phage attacks leading to SVM formation occurred after divergence of phytoplasmas from acholeplasmas, triggering evolution of the phytoplasma clade.

Snowdrift game dynamics and facultative cheating in yeast Nature
The origin of cooperation is a central challenge to our understanding of evolution1, 2, 3. The fact that microbial interactions can be manipulated in ways that animal interactions cannot has led to a growing interest in microbial models of cooperation4, 5, 6, 7, 8, 9, 10 and competition11, 12. For the budding yeast Saccharomyces cerevisiae to grow on sucrose, the disaccharide must first be hydrolysed by the enzyme invertase13, 14. This hydrolysis reaction is performed outside the cytoplasm in the periplasmic space between the plasma membrane and the cell wall. Here we demonstrate that the vast majority (99 per cent) of the monosaccharides created by sucrose hydrolysis diffuse away before they can be imported into the cell, serving to make invertase production and secretion a cooperative behaviour15, 16. A mutant cheater strain that does not produce invertase is able to take advantage of and invade a population of wild-type cooperator cells. However, over a wide range of conditions, the wild-type cooperator can also invade a population of cheater cells. Therefore, we observe steady-state coexistence between the two strains in well-mixed culture resulting from the fact that rare strategies outperform common strategies—the defining features of what game theorists call the snowdrift game17. A model of the cooperative interaction incorporating nonlinear benefits explains the origin of this coexistence. We are able to alter the outcome of the competition by varying either the cost of cooperation or the glucose concentration in the media. Finally, we note that glucose repression of invertase expression in wild-type cells produces a strategy that is optimal for the snowdrift game—wild-type cells cooperate only when competing against cheater cells.

Siderophore production and biofilm formation as linked social traits ISME
The virulence of pathogenic microbes can depend on individual cells cooperating in the concerted production of molecules that facilitate host colonization or exploitation. However, cooperating groups can be exploited by social defectors or ‘cheats’. Understanding the ecology and evolution of cooperation is therefore relevant to clinical microbiology. We studied two genetically linked cooperative traits involved in host exploitation by the opportunistic human pathogen Pseudomonas aeruginosa. Clones that defected from cooperative production of iron-scavenging siderophores were deficient in biofilm formation. The presence of such clones in mixed biofilms with a wild-type clone led to reduced biofilm mass. The fitness advantage of siderophore-deficient mutants in the presence of wild-type bacteria was no greater in biofilm than in planktonic culture, suggesting that these mutants did not gain an additional advantage by exploiting wild-type biofilm polymer. Reduced biofilm formation therefore represents a pleiotropic cost of defection from siderophore production.

Widespread Lateral Gene Transfer from Intracellular Bacteria to Multicellular Eukaryotes Science
Although common among bacteria, lateral gene transfer—the movement of genes between distantly related organisms—is thought to occur only rarely between bacteria and multicellular eukaryotes. However, the presence of endosymbionts, such as Wolbachia pipientis, within some eukaryotic germlines may facilitate bacterial gene transfers to eukaryotic host genomes. We therefore examined host genomes for evidence of gene transfer events from Wolbachia bacteria to their hosts. We found and confirmed transfers into the genomes of four insect and four nematode species that range from nearly the entire Wolbachia genome (>1 megabase) to short (<5>Prisoner's dilemma in an RNA virus Nature
The evolution of competitive interactions among viruses was studied in the RNA phage phi6 at high and low multiplicities of infection (that is, at high and low ratios of infecting phage to host cells). At high multiplicities, many phage infect and reproduce in the same host cell, whereas at low multiplicities the viruses reproduce mainly as clones. An unexpected result of this study was that phage grown at high rates of co-infection increased in fitness initially, but then evolved lowered fitness. Here we show that the fitness of the high-multiplicity phage relative to their ancestors generates a pay-off matrix conforming to the prisoner's dilemma strategy of game theory. In this strategy, defection (selfishness) evolves, despite the greater fitness pay-off that would result if all players were to cooperate. Viral cooperation and defection can be defined as, respectively, the manufacturing and sequestering of diffusible (shared) intracellular products. Because the low-multiplicity phage did not evolve lowered fitness, we attribute the evolution of selfishness to the lack of clonal structure and the mixing of unrelated genotypes at high multiplicity.

Bacteriophages Encode Factors Required for Protection in a Symbiotic Mutualism Science
Bacteriophages are known to carry key virulence factors for pathogenic bacteria, but their roles in symbiotic bacteria are less well understood. The heritable symbiont Hamiltonella defensa protects the aphid Acyrthosiphon pisum from attack by the parasitoid Aphidius ervi by killing developing wasp larvae. In a controlled genetic background, we show that a toxin-encoding bacteriophage is required to produce the protective phenotype. Phage loss occurs repeatedly in laboratory-held H. defensa–infected aphid clonal lines, resulting in increased susceptibility to parasitism in each instance. Our results show that these mobile genetic elements can endow a bacterial symbiont with benefits that extend to the animal host. Thus, phages vector ecologically important traits, such as defense against parasitoids, within and among symbiont and animal host lineages. [My less technical explanation]

Evidence for an early prokaryotic endosymbiosis Nature
Endosymbioses have dramatically altered eukaryotic life, but are thought to have negligibly affected prokaryotic evolution. Here, by analysing the flows of protein families, I present evidence that the double-membrane, Gram-negative prokaryotes were formed as the result of a symbiosis between an ancient actinobacterium and an ancient clostridium. The resulting taxon has been extraordinarily successful, and has profoundly altered the evolution of life by providing endosymbionts necessary for the emergence of eukaryotes and by generating Earth's oxygen atmosphere. Their double-membrane architecture and the observed genome flows into them suggest a common evolutionary mechanism for their origin: an endosymbiosis between a clostridium and actinobacterium.

***Timing of transmission and the evolution of virulence of an insect virus Proc Biol Sci.
We used the nuclear polyhedrosis virus of the gypsy moth, Lymantria dispar, to investigate whether the timing of transmission influences the evolution of virulence. In theory, early transmission should favour rapid replication and increase virulence, while late transmission should favour slower replication and reduce virulence. We tested this prediction by subjecting one set of 10 virus lineages to early transmission (Early viruses) and another set to late transmission (Late viruses). Each lineage of virus underwent nine cycles of transmission. Virulence assays on these lineages indicated that viruses transmitted early were significantly more lethal than those transmitted late. Increased exploitation of the host appears to come at a cost, however. While Early viruses initially produced more progeny, Late viruses were ultimately more productive over the entire duration of the infection. These results illustrate fitness trade-offs associated with the evolution of virulence and indicate that milder viruses can obtain a numerical advantage when mild and harmful strains tend to infect separate hosts.

***Virulence-transmission trade-offs and population divergence in virulence in a naturally occurring butterfly parasite PNAS
Why do parasites harm their hosts? Conventional wisdom holds that because parasites depend on their hosts for survival and transmission, they should evolve to become benign, yet many parasites cause harm. Theory predicts that parasites could evolve virulence (i.e., parasite-induced reductions in host fitness) by balancing the transmission benefits of parasite replication with the costs of host death. This idea has led researchers to predict how human interventions—such as vaccines—may alter virulence evolution, yet empirical support is critically lacking. We studied a protozoan parasite of monarch butterflies and found that higher levels of within-host replication resulted in both higher virulence and greater transmission, thus lending support to the idea that selection for parasite transmission can favor parasite genotypes that cause substantial harm. Parasite fitness was maximized at an intermediate level of parasite replication, beyond which the cost of increased host mortality outweighed the benefit of increased transmission. A separate experiment confirmed genetic relationships between parasite replication and virulence, and showed that parasite genotypes from two monarch populations caused different virulence. These results show that selection on parasite transmission can explain why parasites harm their hosts, and suggest that constraints imposed by host ecology can lead to population divergence in parasite virulence.

The Selection Landscape of Malaria Parasites Science
Malaria parasites have to survive and transmit within a highly selective and ever-changing host environment. Because immunity to malaria is nonsterilizing and builds up slowly through repeated infections, commonly the parasite invades a host that is immunologically and physiologically different from its previous host. During the course of infection, the parasite must also keep pace with changes in host immune responses and red-blood-cell physiology. Here, we describe the “selection landscape” of the most virulent of the human malaria parasites, Plasmodium falciparum, and the adaptive mechanisms it uses to navigate through that landscape. Taking a cost-benefit view of parasite fitness, we consider the evolutionary outcomes of the most important forces of selection operating on the parasite, namely immunity, host death, drugs, mosquito availability, and coinfection. Given the huge potential for malaria parasite evolution in the context of the recently renewed effort to eradicate malaria, a deeper understanding of P. falciparum adaptation is essential.

***Lenski Historical contingency and the evolution of a key innovation in an experimental population of Escherichia coli PNAS
The role of historical contingency in evolution has been much debated, but rarely tested. Twelve initially identical populations of Escherichia coli were founded in 1988 to investigate this issue. They have since evolved in a glucose-limited medium that also contains citrate, which E. coli cannot use as a carbon source under oxic conditions. No population evolved the capacity to exploit citrate for >30,000 generations, although each population tested billions of mutations. A citrate-using (Cit+) variant finally evolved in one population by 31,500 generations, causing an increase in population size and diversity. The long-delayed and unique evolution of this function might indicate the involvement of some extremely rare mutation. Alternately, it may involve an ordinary mutation, but one whose physical occurrence or phenotypic expression is contingent on prior mutations in that population. We tested these hypotheses in experiments that “replayed” evolution from different points in that population's history. We observed no Cit+ mutants among 8.4 × 1012 ancestral cells, nor among 9 × 1012 cells from 60 clones sampled in the first 15,000 generations. However, we observed a significantly greater tendency for later clones to evolve Cit+, indicating that some potentiating mutation arose by 20,000 generations. This potentiating change increased the mutation rate to Cit+ but did not cause generalized hypermutability. Thus, the evolution of this phenotype was contingent on the particular history of that population. More generally, we suggest that historical contingency is especially important when it facilitates the evolution of key innovations that are not easily evolved by gradual, cumulative selection.

***Optimization of DNA polymerase mutation rates during bacterial evolution PNAS
Mutation rate is an important determinant of evolvability. The optimal mutation rate for different organisms during evolution has been modeled in silico and tested in vivo, predominantly through pairwise comparisons. To characterize the fitness landscape across a broad range of mutation rates, we generated a panel of 66 DNA polymerase I mutants in Escherichia coli with comparable growth properties, yet with differing DNA replication fidelities, spanning 10(3)-fold higher and lower than that of wild type. These strains were competed for 350 generations in six replicate cultures in two different environments. A narrow range of mutation rates, 10- to 47-fold greater than that of wild type, predominated after serial passage. Mutants exhibiting higher mutation rates were not detected, nor were wild-type or antimutator strains. Winning clones exhibited shorter doubling times, greater maximum culture densities, and a growth advantages in pairwise competition relative to their precompetition ancestors, indicating the acquisition of adaptive phenotypes. To investigate the basis for mutator selection, we undertook a large series of pairwise competitions between mutator and wild-type strains under conditions where, in most cases, one strain completely overtook the culture within 18 days. Mutators were the most frequent winners but wild-type strains were also observed winning, suggesting that the competitive advantage of mutators is due to a greater probability of developing selectably advantageous mutations rather than from an initial growth advantage conferred by the polymerase variant itself. Our results indicate that under conditions where organism fitness is not yet maximized for a particular environment, competitive adaptation may be facilitated by enhanced mutagenesis.

Different Trajectories of Parallel Evolution During Viral Adaptation Science
The molecular basis of adaptation is a major focus of evolutionary biology, yet the dynamic process of adaptation has been explored only piecemeal. Experimental evolution of two bacteriophage lines under strong selection led to over a dozen nucleotide changes genomewide in each replicate. At least 96 percent of the amino acid substitutions appeared to be adaptive, and half the changes in one line also occurred in the other. However, the order of these changes differed between replicates, and parallel substitutions did not reflect the changes with the largest beneficial effects or indicate a common trajectory of adaptation.

***Competitive fates of bacterial social parasites: persistence and self-induced extinction of Myxococcus xanthus cheaters Proc Biol Sci.
Cooperative biological systems are susceptible to disruption by cheating. Using the social bacterium Myxococcus xanthus, we have tested the short-term competitive fates of mixed cheater and wild-type strains over multiple cycles of cooperative development. Cheater/wild-type mixes underwent several cycles of starvation-induced multicellular development followed by spore germination and vegetative population growth. The population sizes of cheater and wild-type strains in each pairwise mixture were measured at the end of each developmental phase and each growth phase. Cheater genotypes showed several distinct competitive fates, including cheater persistence at high frequencies with little effect on total population dynamics, cheater persistence after major disruption of total population dynamics, self-extinction of cheaters with wild-type survival, and total population extinction. Our results empirically demonstrate that social exploitation can destabilize a cooperative biological system and increase the risk of local extinction events.

***Triassic origin and early radiation of multicellular volvocine algae PNAS
Evolutionary transitions in individuality (ETIs) underlie the watershed events in the history of life on Earth, including the origins of cells, eukaryotes, plants, animals, and fungi. Each of these events constitutes an increase in the level of complexity, as groups of individuals become individuals in their own right. Among the best-studied ETIs is the origin of multicellularity in the green alga Volvox, a model system for the evolution of multicellularity and cellular differentiation. Since its divergence from unicellular ancestors, Volvox has evolved into a highly integrated multicellular organism with cellular specialization, a complex developmental program, and a high degree of coordination among cells. Remarkably, all of these changes were previously thought to have occurred in the last 50–75 million years. Here we estimate divergence times using a multigene data set with multiple fossil calibrations and use these estimates to infer the times of developmental changes relevant to the evolution of multicellularity. Our results show that Volvox diverged from unicellular ancestors at least 200 million years ago. Two key innovations resulting from an early cycle of cooperation, conflict and conflict mediation led to a rapid integration and radiation of multicellular forms in this group. This is the only ETI for which a detailed timeline has been established, but multilevel selection theory predicts that similar changes must have occurred during other ETIs.
posted by Blasdelb at 12:04 PM on October 8, 2012 [74 favorites]


Scientist: but that mutation rates themselves are targets of selection such that a population of organisms might evolve to have higher or lower mutation rates depending on environmental factors.
Brilliant.
posted by IAmBroom at 12:29 PM on October 8, 2012


Fuck I totally forgot to add, the coolest part of Lenski's research is that it is a quantitative analysis of a Nobel Prize winning experiment from back in the 40s, which was at the time in a lot of ways the biggest thing to happen in evolutionary biology since Darwin but few remember.
posted by Blasdelb at 12:38 PM on October 8, 2012 [3 favorites]


"I should say that his work also speaks to the value of the kind of long-term, longitudinal studies that are so hard to get funded these days. Lenski can get grants to keep doing what he does because at this point he has a sterling track record of producing great research, but it's not an easy thing to get support for a career that involves doggedly pursuing the same set of questions in the same way for decades on end and which only starts yielding really interesting data around Year Ten."

This experiment wasn't really funded, at least not directly. It was really an afterthought that may or may not have struck gold, which was tagged on to a bunch of other experiments that were being done on the same flasks.

"He has a couple of papers which explore the idea that not only is mutation a primary driver of evolution, but that mutation rates themselves are targets of selection such that a population of organisms might evolve to have higher or lower mutation rates depending on environmental factors. Heady stuff. His poor students though, inoculating cell culture after cell culture, ad infinitum. It's tedious but very valuable and fruitful work."

You may shit your pants loving this paper, damn is it beautiful.
posted by Blasdelb at 12:45 PM on October 8, 2012 [7 favorites]


Given this: We show that, as predicted by the theory, sex increases the rate of adaptation to a new harsh environment but has no measurable effect on fitness in a new benign environment -- it would seem that sex is a fairly positive adaptation, it costs some energy, increases the mutation rate in a beneficial way, and only costs a little in energy.

It's seems odd, then, that in so many species (particularly insects), sex turns out to have rather unfortunate side effects for one of the partners.
posted by CheeseDigestsAll at 1:01 PM on October 8, 2012


Holy hell Blasdelb, nice work. Something to chew through next time I'm waiting for a gel to run, that's for sure. I see you decided to drop Muller's ratchet right off the bat, that's a bold move. Well done. For anyone who might be blinded by the wall of text that Blasdelb just threw down (but you should really at least try to read it because there are definitely a lot of mind-blowingly awesome ideas in the papers he highlights, albeit one could probably spend several days chewing on any one of them) here is my stab at a lay summary of what I think is one of the most interesting ideas in microevolution:

Muller's ratchet is a negative consequence of asexual reproduction. Asexually reproducing organisms pass their entire genome down to their descendents, essentially unmodified. Unmodified, that is, except for the fact that any random mutations that may have happened either over the course of the parent organism's lifespan or during the process of reproduction are also transmitted to the parent organism's progeny.

In sexually-reproducing organisms, these mutations might be removed from the population later through crossing over of chromosomes, which is where the chromosomes of a cell that is destined to turn into eggs or sperm swap bits of themselves back and forth, shuffling the genes. This process of crossing over allows a deleterious mutation (a mutation with a negative effect on fitness) to be essentially deleted, allowing the chance to pass on the rest of the chromosome (which might be perfectly good, and might even have some novel adaptations on it) without also passing on the deleterious mutation.

This mechanism does not exist in asexual reproduction. Asexually reproducing organisms, as I mentioned above, have to pass on their entire genome and have no mechanism for removing mutations (except for a fortuitous reverse mutation, which does happen but is statistically unlikely). Since any random mutation has a much higher chance of being deleterious (bad) than being adaptive (good), this means that negative mutations will pile up in the descendants of an asexually-reproducing lineage much faster than positive ones.

This process is called Muller's ratchet after Hermann Joseph Muller, with the ratchet part indicating the fact that the process only moves one way. In the absence of other factors, deleterious mutations pile up in asexual lineages, increasing the "genetic load" of the descendents. Over time this can have a severe negative effect on fitness. The only way to remove those mutations is to delete those sequences entirely from the genome (which does happen, and causes such genomes to shrink over time -- you can probably figure out why this isn't a perfect solution) or to delete those entire lineages from the population, causing populations or in theory entire species to become extinct.

Interestingly, it also acts on non-recombining portions of sexually-reproducing organisms' genomes, such as the human Y chromosome (which only comes in a single copy, and therefore has nothing to recombine with) and may explain why said chromosome is so much smaller than the others.

Am I the only person who thinks that is so cool?
posted by Scientist at 1:07 PM on October 8, 2012 [8 favorites]


The best part of that paper? Viruses can be clearly demonstrated to have orgies, and they are so much sexier than anything we can do.
posted by Blasdelb at 1:15 PM on October 8, 2012


Zimmer's writing on this has been excellent. Thanks for this post, CheeseDigestsAll.
posted by homunculus at 1:37 PM on October 8, 2012


Speaking of the Nobels: Nobel awarded for stem cell reprogramming - Pair showed that adult cells can be reprogrammed to an embryonic state.
posted by homunculus at 1:38 PM on October 8, 2012 [1 favorite]


Interestingly, it also acts on non-recombining portions of sexually-reproducing organisms' genomes, such as the human Y chromosome (which only comes in a single copy, and therefore has nothing to recombine with) and may explain why said chromosome is so much smaller than the others.

Am I the only person who thinks that is so cool?

When reading your explanation I was cringing out of a general "hey, poor asexually-reproducing organisms" sense of commiseration until I saw it applies to Y chromosomes. Splendid :/

But it's cool that every time there's a scientific thread here someone will explain the subject or something tangential to it. I usually look out for that and maybe the absense of such explanations is why modern-art threads go pear shaped, but explaining subjectivity is hard.
posted by ersatz at 3:43 PM on October 8, 2012


This fpp and the ensuing discussion are both pure win. Bravo.
posted by AElfwine Evenstar at 5:06 PM on October 8, 2012


Man is this some good stuff. It will take me forever to puzzle through it, but I will persevere, simply because of those wonderful 'ah ha!" moments. Lenski is one of my heroes.


...leaves only two options: acceptance and willfully plugging one's ears. Some people will pick option two, but that takes a certain amount of effort to sustain. On some level, they now know.

And some people are so full of crap their ears are permanently plugged. I was trying to tell someone I know about this post and how great it was, and their college-educated self just blew me off. I told them I'd forward the links, which contain the scientific abstracts and other information. Their response: "Pffft, you can say anything with words, but it doesn't prove anything." How the heck can you respond to that? except maybe with a large rock on their head.
posted by BlueHorse at 6:17 PM on October 8, 2012


Here is a pretty paired down collection of Blasdelb's favorite papers in microbial evolution

WOW! Doubleplusgood, Blasdelb. Thanks very much for these links.

Here is my own pitiful contribution.
posted by dmayhood at 6:36 PM on October 8, 2012 [3 favorites]


CheeseDigestsAll: It's seems odd, then, that in so many species (particularly insects), sex turns out to have rather unfortunate side effects for one of the partners.
Nature is red in tooth and claw.

Or, IOW: fuck them (first literally, then figuratively), the progeny are all that matter.
posted by IAmBroom at 2:15 PM on October 9, 2012


Yessss, this experiment is awesome.

(And that Conservapedia exchange is hilarious. Particularly this, from Schlafly: "I particularly request access to the data that was made available to the peer reviewers of your paper... As before, I'm requesting the organized data themselves, not the graphs and summaries set forth in the paper and referenced in your first reply to me." i.e., I HAVE NO IDEA WHAT THE FUCK I AM TALKING ABOUT.)
posted by en forme de poire at 4:41 PM on October 9, 2012


Came for Blasdelb's links, stayed for the scientific smackdown on this Conservapedia thing.

As before, I'm requesting the organized data themselves, not the graphs and summaries set forth in the paper and referenced in your first reply to me." i.e., I HAVE NO IDEA WHAT THE FUCK I AM TALKING ABOUT.)

I also have no idea what the fuck I am talking about, but it seemed to me that Lenski performed a crude sleight of hand by suddenly reframing the data request as a request for the 'living' data, ie the microorganisms, and then derided Schlafly's E.Coli handling abilities.

I didn't read the paper either, but surely between the bugs and the graphs falls the shadow of a metric fuckton of tedious observational data - 20 years of measurements & dissections & microscope photographs & DNA analysis & CSI stuff like that...?

Why not just flood this Schlafly guy with raw data so deep, that he'll have no option in the end but to emerge grasping an olive branch of peace?
posted by UbuRoivas at 2:12 AM on October 12, 2012


All of the raw data, the mountains, exist in lab notebooks on a couple of shelves in his lab. To transcribe all of the into a form Schafly could examine would be a massive undertaking. He seems to mean something more processed than that, but he doesn't specify what thing he means exactly, which makes the request functionally impossible to fulfill.
posted by Blasdelb at 2:30 AM on October 12, 2012


Which, I suppose, was Schlafly's strategy all along, if I credit him with even half a brain: demand data that he knows cannot realistically be provided, then accuse Lenski of obfuscating when he inevitably fails to deliver.
posted by UbuRoivas at 2:58 AM on October 12, 2012 [1 favorite]


Yeah, my point above was that peer reviewers only have access to the data as it is presented in the paper. Certainly none of them looked at like, scans from a dude's notebook.

And also, as a side note, implying that these graphs aren't a faithful representation of the contents of Lenski's grad student's lab notebook is a pretty serious accusation. It would basically mean that they had committed straight-up fraud or at least grave misconduct.
posted by en forme de poire at 10:31 AM on October 12, 2012


(And actually, there are some people who digitize and upload their entire lab notebooks - but as Blasdelb said it's nowhere near standard practice and for a 30-year-old experiment it would be a hell of an undertaking.)
posted by en forme de poire at 10:39 AM on October 12, 2012


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